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61 Cards in this Set
- Front
- Back
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Characteristics of Inflammation
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1. Redness- blood vessels dilation
2. Swelling- leakage of fluid/ imflammatiory cells from blood vessels 3. Heat- inc blood flow 4. Pain- stretch/distortion of inflamed tissue |
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Rhinitis
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- inflammation of nasal mucosa
- due to allergic rxn to pollen, house dust, mites, mold, spores, animal dander Sympt: (throat eyes ears) 1. Runny nose 2. Nasal congestion 3. Sneezing 4. Itching 5. Postnasal drainage |
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Main cause of rhinitis
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Histamine, other inflammatory agents --> increase
1. mucous 2. fluid secretion 3. congestion (swelling) |
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"Hay fever"
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-air born pollen (mold or fungus) allergy, seasonal allergic rhinitis or pollinosis
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Sinusitis
Definition Results from? |
- inflammation of mucous membranes of 1 or more paranasal sinuses --> accompanies rhinitis
blockage of sinus drainage-> result from bacterial prolif--> inflammation sinus mucosa |
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Sinusitis
Symptoms |
1. pain
2. Pressure over affected sinus 3. Purulent mucous secretion (pus) 4. Occasional fever Acute: start cold --> 3 weeks Chronic: 3-8 weeks can be months --> years |
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Sinusitis
Causes |
- any condition that blocks drainage or aeration of involved sinus
(virus, rhinitis, septal deviation.. etc) - Streptococcus pneumonia or haemophilus influenza with blocked sinuses /low resistance--> bacteria multiply |
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Sinusitis
Diagnosis Treatment |
- chronic sinusitis from persistent sympt , examin purulent discharge (pus) radio graph examination
Tx: decongestants, antibiotics, pain relievers |
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Tonsils form a ring of ____ just beyond the oral cavity
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lymphoid tissue
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Tonsillitis
Definitions/ Which tonisils Where from? |
- inflammation of tonsils
Mainly 1. palatine (more commonly affected) 2. Pharyngeal or both Due to virus (preschoolers) bacterium (older kids) |
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Acute tonsillitis
Chronic Tonsillitis |
Acute:
last 4-6 days Children 5-10 y/o Chronic: recurrent episodes (3-4x/yr) of tonsillar infection (despite antibiotic therapy) tonsils surgically removed - lead to ear infection/hearing loss (obstruction eustachian tube) |
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Tonsillitis
Symptoms |
1. sore throat
2. voice changes 3. dysphagia (swallowing difficult) 4. fever 5. Malaise 6. Swollen neck lymph nodes 7. adenoids are inflammed --> mouth breathing bc airway blocked |
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Treatment for
Bacterial tonsillitis Viral tonsillitis |
Bacterial:
treated with antibiotics Viral: supportive measurements Fluid intake, salt water gargles, rest |
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Tonsillitis
Bacterium that causes it Virus that causes it |
Group A beta-hemolytic steptococcus
"strep throat" Virus: Coxackie Epstein Barr |
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Adenoids- Tonsillitis
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Chidlrens adenoids grow 3-5 yrs after they shrink --> disappear by puberty
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COPD
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- restriction of airflow in lungs
- most common gr of chronic lung dieases - cause tobaccos smoke Inc: 1. chronic bronchitis 2. emphysema 3. chronic asthma |
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Bronchitis
Definition How does it happen? |
- respiratory disease
- mucosa of bronchi bc inflammed - inflammation --> swelling mucous membranes --> narrow airway passages--> excessive mucous production --> cillary loss |
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Acute Bronchitis
Who does it affect? Treatment? |
- last < 2 weeks
- all ages (more kids/old) - not a disease of COPD (chronic form is) - usually self limited with eventual healing and return of normal respiratory func |
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Acute bronchitis
Causes? Where does it develop from? |
90% --> virus
10% --> bacteria develops after viral cold, flu, etc,= Made worst by smoking , allergies, noxious air born pollutants/irritants |
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Acute bronchitis
Symptoms |
- persistent hacking cough with phlegm
- fatigue - low grade fever not above 38.9 - diff breathing, some wheezing |
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Chronic bronchitis
What happens if its chronic |
- mucosal inflammation
- swelling - hypertrophy - hyperplasia of sero-mucous glands chronic irritation and inflammation --> firbosis and thickening of bronchial wall --> more airway obstruction Airway obstruction --> impaired gas exchange - not fully reversible, progresses slowly over years - coexist with emphysema/asthma |
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Chronic bronchitis
Symptoms |
1. dyspnea- SOB
2. tachypena- rapid breathing 3. wheezing 4. fatigue 5. freq respiratory infections 6. HA 7. persistent cough 8. hypoxia - dec O2 content in blood and tissue 9. cyanosis- bluish/purple skin 10. hypercapnia (inc CO2 conc) |
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Chronic bronchitis
Treatments |
- reduce exposure to irritants
- prompt med txt - use expectorants (inc mucous sec and its expulsion) - bronchodilators - app chest therapy to remove mucous secretion -low flow oxygen - nutritional supplemetnation |
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Emphysema
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- pathological change is breakdown of alveolar walls --> enlarge permanently inflated alveoli
- 4th leading cuase of death with chronic bronchitis and asthma |
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Emphysema
Causation factors |
1. genetic deficiency of alpha1-antitrypsin (AAT) --> inhibits protease activity
2. Cigarette smoking (>80% of cases) --> dec AAT activity 3. bacterial release of proteases; asthmatics, TB, coal dust |
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Emphysema
How it works? |
Protease (elastase) breakdown alveolar walls --> loss of capilaries --> loss in SA for gas exchange
-Protease--> lose of elastic fibers affect elastic recoil during expiration--> diff expiration - dec mechanical support of small bronchi --> collapse and obstruction of air flow - fibrosis/ thickening of bronchial walls --> more obstruction |
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Emphysema
Symptoms |
1. dyspnea- shortness of breath
2. cough 3. wheezing 4. chornic mucous production 5. hyperventilation 6. anorexia (diminished appetite) and fatigue |
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Advance emphysema
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- adj damaged alveoli coalesce to form large holdes --> blebs or bullae
--> pneumothorax --> hypercapnia (excess CO2 in blood) - infections develop frequently bc secretions are more diff to remove - airway defense are impared |
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Emphysema
Treatment |
- avoiding respiratory irritants and sources of respiratory infections
- breathing excercises - good nutrition--> hydration - bronchodilators - antibiotics - possible oxygen therapy |
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Asthma
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- widespread narrowing of airways (small bronchi and bronchioles) in response to various stimuli
- period episodes of severe but reversible bronchial obstructions wtih hypersensitive or hyper-responsive airways - freq atacks of acute asthma --> irreversible damage --> chronic asthma |
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Asthma
Symptoms |
- cough with thick productive mucous
-dyspnea, rapid and labored breathing - tight chest - wheezing/agitation - no txt, tachychardia, hypoxemia, respiratory failure by cyanosis, inc blood CO2 |
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Extrinsic Asthma
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- allergic asthma
- mostly in children, triggered by Type I hypersensitivity rxn to inhaled antigen - seasonal with elevated levels of IgE |
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Extrinsic Asthma
Risk Factors |
1. hereditary predispostion
2. viral infections before 2 3. exposure to common allergens like dust mites, animal dander, cockroaches |
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Intrinsic (Nonallergic) Asthma
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- in adulthood
Stimuli: 1. respiratory infection 2. cold exposure 3. drugs like aspirin 4. NSAIDS 5. stress 6. Cigarette smoke - ppl have combo of extrinsic/ intrinsic |
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Extrinsic and Intrinsic Pathology
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- obstructed bronchi and bronchioles due to SM contraction --> inflammed and swollen mucosa--> inc mucous
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Asthma
Treatment |
- minimize number of asthmatic attacks in order to prvent permanent lung damage, reduce risk of infection/ develop COPD
- use inhalers (bronchodilators) - breathing exercise - steroids - other drugs |
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Acute Respiratory Distress Syndrome
aka. Infant/Neonatal Respiratory Distress syndrom (IRDS/ NRDS) aka. Hyaline Membrane disease |
- found in premature infants
- due to insufficient surfactant secretion from Type II alveolar cells |
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Infant Respiratory Distress Syndrome
What dose it affect? |
- basic defect is inc alveolar surface tension causing alveolar collapse
1. Poor lung perfusion (blood circulation) 2. lack of surfactant 3. formation of fibrin-rich 4. protein- rich exudate (hyaline membrane) 5. altelectasis (loss of alveolar air and alveolar collapse) 6. reflex pulmonary vasoconstriction 7. Severe hypoxia --> brain damage |
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Infant Respiratory Distress
Treatment |
1. corticosteroids
2. Synthetic surfactant 3. Mechanical ventilation 4. Oxygen therapy |
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Cystic Fibrosis (CF)
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- common fatal genetic disorder
(1/3,300 caucasian) - primary effect is on pancreas/lungs - live to 40 y.o - exocrine glands (salivary, sweat, pancreas) reproductive sys ducts, bronchioles, bronchi --> thick mucous secretions --> obstruction |
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Cystic Fibosis (CF)
CFTR- cystic fibrosis transmembrane |
- coded on chromosome 7
- regulates transport of salt and water in/out of cell |
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Cystic fibrosis
In the lungs |
- mucous obstructs air flow in bronchioles and small bronchi which causes air to be trapped with permanent damage to bronchial walls
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Cystic firbosis
How it works? |
- mucous is stagnant --> bacteria proliferate --> cause progressive destruction of lung tissue
- --> respiratory failure or cor pulmonale (R side congestive heart failure) developes |
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Cystic Fibrosis
Bronchiectasis |
- (chronic dialtion of bronchi or bronchioles) and emphysematous changes seen freq as fibrosis and obstructions advance
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Cystic Fibrosis
Symptoms |
1. Salty taste to sweat due to excess NaCl
2. Malabsorption due to lack of pancreatic enzymes 3. Chronic cough due to excess mucous 4. Freq respiratory infections due to excess bacterial growth 5. Hypoxia, fatigue and excercise intolerance 6. Failure to reach growth expectations |
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Cystic Fibrosis
Treatment |
1. Interdisciplinary team approach bc mult sys involved
2. Replacement therapy (pancreatic enzymes and bile salts) 3. Nutritional/ vitamin balance 4. hydration 5. Chest pysiotherapy 6. Bronchodilators and humidifers 7. antibiotics 8. oxygen therapy for advanced disease |
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Pneumonia (Pneumonitis)
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- inflammation/congestion of the lower respiratory tract --> area of gas exchange alveoli
- characterized by alveolar air spaces or alveolar walls filled with exudates (fluid escaping from alveolar caps), macrophages read and white blood cells and fibrin 2 categories: community acquired (most common) and hospital acquired (nosocomial) |
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Pneumonia
Caused by |
infection by bacteria or virusses
few due to inhalation of chemicals or trauma to the chest wall small minority to fungi and yeast |
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Pneumonia
How does it work |
- Normal: small particles inhaled--> sensors along repiratory tract trigger coughing /sneezing --> force them out
- tiny ones are trapped in mucous coat and moved out of repiratory path by cilary movement - bacteria or other infections agents that make their way to alveoli are attacked by alveolar macrophages - if latter defenses are weakened or damaged --> pneumonia |
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Pneumonia
When does it occur |
- when defense system is weakened by another illness like.. viral upper respiratory infection (URI) or influenza
- organisms enter lung by aspiration (breathing in secretions of virus) by resident bacteria spreading along the mucosa or by aspirating vomitus |
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Lobular pneumonia
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-occurs in one lobe or more lobes
- due to Streptococcus pneumoniae (penumococcus) - can be from staphylococcus aureus and legionella (Legionnaires disease) - cause accumulation of alveolar exudate forming a solid mass in lobe --> consolidation |
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Pneumonia
Pleuritis or Pleurisy Empyema |
Pleuritis- adjacent pleural membranes involved --> painful
Empyema- when infection spreads to pleural cavity - cause adhesions between pleural membranes restricting ventilation |
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Pneumonia
When alveoli filled with exudate --> reduce gas exchange pts become.. |
hypoxic and dehydrated
(from high fever, hyperventilation and reduced fluids) |
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Hospital acquired (nosocomial) pneumonia
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- affects ppl with less resistance (old)
-debilitated -malnourished - immune suppressed - result from staphylococcus aureus |
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Bronchopneumonia
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-infection which has spread more extensively throughout the lungs
- has diffused or patchy distribution usually involving both lungs -found in lower lungs |
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Bronchopneumonia
How does it work? |
- microorganisms start growing within bronchial mucosa --> spread to alveoli
- pooled secretions in lungs --> become infected by organisms drainign upper passages --> hazard for immobilized pts (hypostatic pneumonia) - antibiotic treatment |
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Legionnaire's Disease
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-pneumonia caused by bacterium Legionella pneumophila
- grows in warm, moist environments like air pipes, spas -mircrobe inhaled with contaminated air--> diff to identify bc organism is found within pulmonary macrophages and req special culture medium for growth - if not treated-->death |
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Primary Atypical Pneumonia (PAP)
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- viral or mycoplasma pneumoniae
- involves interstitial inflammation rather than alveolar consolidation - absense of exudates within alveolar space while alveolar walls are thickend by edema containing lymphocytes, macrophages, plasma cells |
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Primary Atypical Pneumonia (PAP)
Causitive agents |
virus (influenza A or B)
adenoviruses respiratory syncytial virus (RSV) - mild to severe - usually self limiting |
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Pneumocystis Carnii Pneumonia (PCP)
Who does it affect? |
- atypical penumonia occuring as opportunistic and fatal infections
in pts wth -AIDS - babies - post organ transplants with weaken immune system |
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Pneumocystis Carnii Pneumonia (PCP)
What causes it? How does it work? |
- caused by fungus which is inhaled and attaches to alveolar cells causing necrosis and diffuse interstital inflammation
- alveoli fill with exudates and fungi --> difficult breathing |
